Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MBBS II ERS > L10 – Pathology of the Parathyroid Glands > Flashcards

L10 – Pathology of the Parathyroid Glands Flashcards

1
Q

Typical number and anatomical location of parathyroid glands?

A

Range from 3 to 6
Normally 4

Located at upper and lower poles of thyroid gland on each side

could be found along lines of descent from pharyngeal pouch (ectopic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Are parathyroid glands encapsulated into the thyroid gland?

A

Can be over the surface or invaginated into thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

3 main types of parathyroid gland cells? Function?

A

Chief cell = Produce, store, secrete PTH

Oxyphil cells = Function unknown

Water-clear cells = chief cells with accumulated glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Compare staining of chief vs Oxyphil cells in parathyroid gland?

A

Chief = Pale Eosinophilic cytoplasm with vacuoles

Oxyphil = dense, eosinophilic cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal arrangement of Parathyroid gland cells?

A

intermixed in variable proportions

Arranged in nests / trabeculae / acinar

separated by abundant adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of PTH?

A

Decreased free, ionized calcium stimulates parathyroid glands

> > PTH regulate increase calcium levels at:

1) Kidney
2) Bone
3) Intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effect of PTH on Kidneys? (3)

A

Increase distal tubular reabsorption of calcium

Increase PCT phosphate excretion through urine = less phosphate deplete calcium in serum

↑ conversion of vitamin D to 1,25 dihydroxy-D3 = increase calcium absorption from GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Effect of PTH on Bone?

A

Stimulates osteoclastic activity

> > resorb / erode lamellar bones

> release, mobilize ionized calcium into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effect of PTH on GIT?

A

Stimulated by calcitriol from kidney

> > increase calcium absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common cause of hypercalcemia in adults?**

A

Cancer/malignancies

squamous cell carcinoma of the lung or breast carinoma produce PTH-related protein (PTHrP)

> > Bind to PTH receptor

> > exerts effects like PTH on kidneys, bones (without increase in PTH)

> > hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define primary hyperparathyroidism?

A

(excess secretion of PTH in the absence of any known stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary hyperparathyroidism: male or female affected more?

A

Female predom.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Symptoms of primary hyperparathyroidism?

A

Mostly asymptomatic

 Bone pain, fractures
 Renal colic (stones)
 Polyuria, polydipsia (excessive thirst / excess drinking)
 Constipation, nausea
 Peptic ulcers, pancreatitis, gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CNS effects of primary parathyroidism?

A

severe, exceptional cases:

 Depression, lethargy
 Seizures
 Weakness, hypotonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serum test results in primary hyperparathyroidism?

A

Increased serum PTH

Increased Ca, Low PO4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathological changes to bones caused by primary hyperparathyroidism?

A
  • Osteopenia = thinning bone cortices
  • Osteitis fibrosa cystica = loss of bone in BM, fibrosis + haemorrhage + cystic chnage
  • BROWN TUMOUR of hyperparathyroidism = aggregates of osteoclastic reactive giant cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which type of tumour closely resembles the pathological appearance of primary hyperparathyroidism?

A

giant cell tumor of bone = similar to brown tumor of hyperparathyroidism

Brown due to old hemoorhage and hemosiderin deposit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Systemic complications of primary hyperparathyroidism?

A

 Nephrolithiasis (urinary tract stones)

 Nephrocalcinosis (interstitial, tubular calcification)

 Metastatic calcification in stomach, lungs, heart, BV, skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Calcification due to primary hyperparathyroidism is identical to dystrophic calcification. T or F?

A

False

Metastatic calcification is not Dystrophic cal.

Dystrophic = calcium deposits are secondary to tissue necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma

85-95%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Define the genetic mutations asso. with Sporadic and Hereditary Parathyroid adenoma?

A

Sporadic = MEN1 +/- Cyclin D1/ PTH rearrangement

Familial = MEN1 or MEN2A

22
Q

List 3 causes of primary hyperparathyroidism?

A
  • parathyroid Adenoma 85% to 95%
  • Primary hyperplasia (diffuse or nodular) 5% to 10%
  • Parathyroid carcinoma 1%
23
Q

What medical history is asso. with sporadic parathyroid adenoma?

A

exposure to ionizing radiation in the childhood, or secondary to lithium therapy

24
Q

List some endocrine lesions caused by MEN1 mutation

A

Parathyroid hyperplasia**

Pituitary adenoma **

Adrenal cortical adenoma** and hyperplasia

(Neuroendocrine tumours in pancreas, duodenum, thymus…)

25
Q

List some endocrine lesions caused by MEN2 mutation?

A

parathyroid hyperplasia** or adenomas;

thyroidmedullary carcinoma

adrenal pheochromocytomas**

26
Q

List some non-endocrine lesions caused by MEN1 mutation

A

angiofibromas, collagenomas

lipomas, leiomyomas.

meningiomas, ependymomas,

27
Q

Gross appearance of parathyroid adenoma?

A

well-circumscribed, soft, tan nodular mass

thin, delicate capsule

Other normal parathyroid glands are feedback inhibited by Ca&raquo_space; shrink

28
Q

Histological appearance of Parathyroid adenoma?

A

predominantly of chief cells, acinar structure/ admixture

Severe nuclear atypia but not malignant***** (no mitotic figures)

29
Q

Extent of involvement, etiology of parathyroid hyperplasia?

A

Usually diffuse = all 4 glands

Sometimes isolated to 1-2 glands (looks similar to adenoma)

5-25% Hereditary: MEN1 and MEN2A

30
Q

How to tell whether parathyroid hyperplasia is primary or secondary by histology?

A

Primary = Chief cell + water-clear cells hyperplasia

Secondary = Oxyphil cell hyperlasia

31
Q

Histological appearance of parathyroid hyperplasia?

A

DIFFUSE/ MULTINODULAR proliferation

Decrease intraglandular adipose tissue (same as adenoma, tricky to tell apart)

32
Q

Gross appearance of parathyroid carcinoma?

A

Large, weigh >10 g

  1. thick, dense fibrous capsule (gray-white) ** NOT THIN, DELICATE LIKE IN ADENOMA**
  2. Irregular – invasion of surrounding structures, vascular and lymphatic spaces NOT WELL-CIRCUMSIZED LIKE ADENOMA
33
Q

Clinical presentation, extent of involvement and genetic mutation asso. with parathyroid carcinoma?

A

One gland involved

Sporadic or asso. MEN1 and MEN2A

Typical hyperparathyroidism symptoms, death by uncontrolled hypercalcemia

Elevated Serum calcium, PTH, Alkaline phosphatase

34
Q

Histological appearance of parathyroid carcinoma?

A

Trabeculae/ Nodules of Cancer cells***

uniform nuclei with prominent nucleoli

many mitotic figures*** = malignancy

35
Q

List 2 causes of secondary hyperparathyroidism?

A

Chronic renal failure/ insufficiency***

Dietary:

  • Low Vit D
  • Low Calcium
  • Malabsorption of Ca
36
Q

Explain how chronic renal failure leads to secondary hyperparathyroidism?

A
  1. Decreased phosphate excretion = elevated serum phosphate suppress serum calcium
  2. Decrease in α1-hydroxylase activity = less production of calcitriol= less intestinal absorption of calcium

Chronic low Ca = PTH hyperplasia

37
Q

Symptoms of secondary hyperparathyroidism?? *think about underlying cause**

A

KIDNEY FAILURE

  • Fluid/electrolytes imbalance (dehydration, edema, hyperkalemia, metabolic acidosis).
  • Anaemia (Low EPO)
  • Hypertension, uraemic pericarditis.
  • Skin (pruritis, dry skin, hyperpigmentation)
38
Q

Define the serum calcium, phosphate and PTH levels in secondary hyperparathyroidism?

A
  • Serum Ca normal/ slightly low
  • Compensatory increase PTH
  • High PO4
39
Q

Complication of high PO4 in secondary hyperparathyroidism?

A

Calcium phosphate deposit in BV

Narrow BV lumen > ischemia > Calciphylaxis (gangrene)

40
Q

Pathogenesis of tertiary hyperparathyroidism?

A

long-standing secondary hyperparathyroidism

> > prolonged stimulation

> > Chief cell hyperplasia

> > autonomous PTH secretion independent of Ca level

> > very high PTH

41
Q

How to differentiate primary and tertiary hyperparathyroidism?

A

Symptoms: 1° (asymptomatic / renal osteodystrophy) vs. 3°(CRF)

Serum:
Primary = High Ca, Low PO4, High PTH
Tertiary = High Ca, HIGH PO4, VERY HIGH PTH

42
Q

Treatment of tertiary hyperparathyroidism?

A

Parathyroidectomy

43
Q

List 5 causes of Hypercalcaemia with DECREASED PTH?

A
  • Hypercalcemia of malignancy*** (PTH-r protein mediated osteolytic metastases)
  • Vit D toxicity
  • Immobilization
  • Drugs (thiazide)
  • Granulomatous disease (sarcoidosis)
44
Q

Most common causes of hypercalcemia and hypoparathyroidism respectively?

A

Hypercalcemia = Malignancy, PTHrP

Hypoparathyroidism = Iatrogenic most common

45
Q

List 3 causes of hypoparathyroidism?

A
  • Iatrogenic: en bloc parathyroid gland removal surgically (treat thyroid or HNN malig.)
  • Autoimmune: AIRE mutation = AutoAb against endocrine organs
  • Congenital: Di George syndrome ( thymic aplasia and cardiac defects)
46
Q

Clinical manifestation of acute hypoparathyroidism?

A

secondary to hypocalcemia:

C – Convulsion
A – Arrhythmia (irregular heartbeat)
T – Tetany (involuntary contraction of muscles – Chvostek’s sign)
S – Spasm (Trousseau’s sign)

  • Rarely increase ICP and seizures
47
Q

Clinical manifestation of chronic hypoparathyroidism?

A

cataracts,

calcification of the cerebral basal ganglia,

dental abnormalities

48
Q

Expected serum level findings in hypoparathyroidism?

A

Low Ca
High PO4
Low PTH

49
Q

Which type of scan is used to ddx parathyroid adenoma and hyperplasia?

A

technetium-99 radionuclide scan

Hyperplasia: >1 gland will demonstrate increased uptake

> =2 glands are abnormal = favor hyperplasia

50
Q

What procedure is done to examine parathyroid glands for intra-operative dx

A

intraoperative frozen section

Resect gland and store in OCT medium > transfer to cryostat for frozen section dx

51
Q

Define the features seen in intra-operative frozen section of parathyroid glands that favour adenoma vs hyperplasia dx?

A

Adenoma = Visible thin fibrous capsule with a rim of ‘normal’ parathyroid gland tissue

Hyperplasia = >=2 glands are abnormal

Both have decreased fat content: adenoma has almost none

52
Q

Limitations of frozen section dx of parathyroid pathologies?

A
  • Single abnormal gland cannot ddx adenoma and hyperplasia (morphologically same)
  • Capsule is thin, not always visible
  • varying degrees of loss of intra-glandular fat

MBBS II ERS (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions